Cerebrovascular disease (CVD) is considered the second most common cause of mental deterioration in th elderly. Unlike Alzheimer's disease, CVD is treatable. During the first study period, the Stroke and Aging Research Project accomplished its aims to determine the prevalence, incidence, and risk factors for dementia related to stroke, resulting in new information not previously available. The central goals of our proposed continuation are to extend prior findings on risk factors and course using longitudinal studies (Aims l and 2) and to examine new questions on syndromic profiles and anatomic risks using cross-sectional studies (Aims 3 and 4). First, we will identify risk factors for incident dementia in stroke patients initially nondemented at baseline by continued followup of the original cohorts (n=500) and assembly of a new stroke sample (n=300). In our prior study, power was sufficient to identify risk factors based on cross- sectional analysis, but suboptimal for incidence studies. Analysis of existing longitudinal data indicates that power will be sufficient in the proposed study to test the primary hypothesis that cerebral atrophy and recurrent stroke increase the risk of incident dementia. Other factors will be examined as secondary hypotheses. Second, we will characterize the course of cognitive function after stroke. In our prior study, most stroke patients showed a stable or improving course, while some patients showed cognitive decline. The extended followup and larger sample will allow us to test the hypothesis that cardiac disease at baseline is associated with a steeper slope of decline in test scores in some patients. Third, we will examine deficits in executive or frontal lobe function in the new stroke- sample and test the hypothesis that these deficits are more frequent in patients with subcortical compared to cortical infarcts on CT scan. Impaired executive function is considered to be a common manifestation of dementia from subcortical stroke; however, syndrome specificity in relation to lesion type has not been examined in a large stroke cohort. Fourth, we will evaluate an anatomic risk factor for dementia in a subgroup of the new sample with subcortical infarcts and test the hypothesis that involvement of the caudate, anterior capsule-genu, or thalamus is associated with an increased risk of dementia at stroke onset compared to other subcortical locations. In our prior study, some patients presented with a frontal lobe syndrome and dementia from isolated capsular genu infarction, justifying the term "strategic-infarct dementia". Functional imaging suggested that cortical disconnection was a mechanism for dementia, resulting from damage to structures that project to the frontal lobe. Our new anatomic studies will establish the strength of the association. Although dementia is a frequent and disabling consequence of CVD in our rapidly aging population, few studies have examined these issues. Information on syndromes and anatomic risk factors will improve diagnostic precision and clarify pathophysiology. Information on risk factors and course will have preventive implications and may assist in the design of clinical trials aimed at delaying cognitive deterioration. from CVD.